Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PHENTOLAMINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMed1979

Phentolamine and the action of somatostatin in man.

The inhibition by somatostatin (SRIF) of basal and arginine-stimulated glucagon, insulin, and glucose levels was compared with that obtained when SRIF was preceded by alpha-adrenergic blockade with phentolamine. No noteworthy differences were observed, except that the characteristic rebound of insulin upon discontinuation of SRIF was significantly lower with phentolamine (P less than 0.01). These results indicate that inhibition of basal and arginine-stimulated glucagon and insulin secretion by SRIF in man is not mediated through activation by alpha-adrenergic receptors.

Adult↗
PubMed1979

Hemodynamic improvement following a single dose of oral phentolamine. Administration in patients with chronic low output cardiac failure.

Hemodynamic studies were made in 15 patients with chronic low output cardiac failure before and following a single dose of oral phentolamine (150 mg). After two hours significant (P less than .05) reduction occurred in mean pulmonary, wedge and right atrial pressures and increases in cardiac index and heart rate. In ten patients studied at four hours, wedge pressure remained significantly reduced (-18 percent) and cardiac index significantly increased (+19 percent) from control values. Oral phentolamine results in significant hemodynamic improvement in patients with severe heart failure. Duration of effect for at least four hours after a single dose suggests that intermittent oral therapy may be useful in the management of such patients.

Administration, Oral↗
PubMed1990

Prostacyclin but not phentolamine increases oxygen consumption and skin microvascular blood flow in patients with sepsis and respiratory failure.

Inadequate tissue oxygenation may occur in critically ill patients with sepsis despite an apparently adequate O2 transport (QO2), and this may contribute to the development of an O2 debt and also to multiple organ failure. It has been shown that increasing QO2 by infusing a vasodilator may reveal this O2 debt in septic patients. To investigate whether the site of action of vasodilators may be of importance in unmasking such an O2 debt, we administered prostacyclin, a prostaglandin with a preferential effect on the microcirculation, and phentolamine, an arteriolar vasodilator, in 11 patients studied during the first 48 hours after the onset of sepsis, and compared their effect on whole body oxygen consumption (VO2) and skin microvascular blood flow. The results demonstrated that increasing QO2 by prostacyclin but not by phentolamine significantly increases VO2 in critically ill patients with sepsis. The site of action of vasodilators may therefore play an important role in their ability to unmask an O2 debt.

Adult↗
PubMed1979

Neural release of glucagon is inhibited by hyperglycemia and enhanced by phentolamine.

Using an innervated, cross-perfused, canine pancreas-stomach-duodenum preparation, direct neural effects on the immunoreactive glucagon secretion rate (GSR) were separated from blood-borne influences. Both splanchnic nerves were cut above the diaphragm and stimulated simultaneously for three separate 10-min-long periods, twice before and once during a pancreatic arterial phentolamine infusion. The extent of the decreases in GSR that occurred after nerve section was inversely correlated with the arterial plasma glucose concentration at the time of section. Splanchnic nerve stimulation caused a significant increase in GSR. Similar stimulation during a pancreatic arterial phentolamine infusion caused a significantly greater increase. Rapid infusion of glucose near the end of the experiment caused a significant decrease in GSR, demonstrating the responsiveness of the preparation. These data were collected in conjunction with a study of neural influences on insulin secretion rates. It can be concluded that the central nervous system can alter the secretion rate of glucagon by direct neural means. Alpha-adrenergic blockade, in the presence of splanchnic nerve stimulation, enhances GSR.

Animals↗
PubMed1995

Effects of dopamine, dobutamine and phentolamine on middle ear pressure and blood flow in cynomolgus monkeys.

To test the hypothesis that changes in mucosal perfusion could influence gas exchange and thus, middle ear pressure, the effects of systemically administered drugs showing alpha adrenergic effects on mucosal perfusion and middle ear pressure were evaluated in 4 cynomolgus monkeys. Two drugs with well characterized sympathomimetic effects, dopamine and dobutamine, were studied, and dopamine was combined with an antagonist, phentolamine. For each experiment, the monkeys were anesthetized with pentobarbital and followed for a 90 min baseline period. Then, the drug was administered for 60 min with follow-up extending through that period and for an additional 60 min. Data consisted of repeated measurements of rectal temperature, heart rate, blood pressure, left middle ear pressure and right mucosal blood velocity, volume and flow. The results documented an increase in middle ear pressure after intravenous infusion of either dopamine or dobutamine and an attenuation of the response by concurrent administration of phentolamine. Laser Doppler measurements documented a variable, non-directional change in blood volume, velocity and flow. The changes in the middle ear pressure observed following systemic administration of autonomic drugs are consistent with the rapid establishment of a transmucosal pressure gradient secondary to changes in the supply and/or metabolism of gases.

Animals↗
PubMed1975

Effect of phentolamine and propranolol on the survival of experimental skin flaps.

The effect of phentolamine and/or propranolol (alpha- and beta-receptor blocking compounds respectively) on the survival of skin flaps was studied in rats. Phentolamine and/or propranolol were injected intraperitoneally every 12 hours, starting one day before the flap operation, and continued for 5 consecutive days. One week after the operation the survival of the flaps was judged. Systemic treatment with either compound alone or in combination resulted in statistically significant increased survival of the flaps. The results demonstrate that both alpha- and beta-adrenergic receptors influence the survival of skin flaps in rats.

Animals↗
PubMedDate not supplied

The central action of intraventricularly (ivc) administered propranolol and phentolamine in rat.

Propranolol (100mug) ivc together with phentolamine (60 mug) decreased spontaneous locomotor activity and weakened post-nialamide locomotor activity in rat. When applied separately in the above doses, neither of the two compounds had this action. Depression of amphetamine-induced locomotor activity was observed after propranolol (250 mug) together with phetolamine (60 mug). Phentolamine alone, had hypothermic action but when applied together with propranolol, it increased after 4 hrs body temperature. The tested compounds prolonged hexobarbital-induced sleeping time but did not affect noradrenaline or dopamine levels in rat's brain.

Animals↗
PubMed1990

[Investigations on the stability of therapeutic drugs derived from imidazole. XII. Qualitative and quantitative stability evaluation of phentolamine hydrochloride solutions].

Hydrolysis of phentolamine hydrochloride in aqueous solutions, and at pH 1.0 and pH 8.0 was studied by means of thin-layer chromatography. A spectrophotometric method for quantitative assessment of phentolamine hydrochloride hydrolysis has been elaborated, and thermodynamic parameters of this reaction were determined.

Chromatography, Thin Layer↗
PubMed1989

Effects of atropine, acetylsalicylic acid, FPL 55712, and phentolamine on increased histamine responsiveness of cat lung strips under conditions of airway inflammation.

Our recent in vitro studies on airway smooth muscles of cats with turpentine oil inflammation showed an increase of isometric tension of the lung strips to histamine application. This communication describes the effect of atropine, acetylsalicylic acid, FPL 55712, and phentolamine on the histamine contractions of the lung strips derived from control and experimental groups of cats. Pretreatment of the lung strips with atropine and acetylsalicylic acid had no significant effect on histamine induced contraction. FPL 55712 significantly decreased the mean values of isometric contractions after the low doses of histamine in experimental groups of strips. The isometric contractions after higher doses of histamine were not affected by FPL 55712 in both groups of strips. The significant increase of histamine contractions of the lung strips induced by experimental inflammation was reduced by phentolamine. The role of alpha adrenergic receptors in the increased responsiveness of the inflamed lung tissues to histamine is discussed.

Animals↗
PubMed1989

[Effect of phentolamine on the reflex increase in arterial pressure].

Experiments were carried out in anaesthetized and curarized cats to study the effects of the alpha-blocker phentolamine on arterial pressor response to stimulation of group I afferent fibers from gastrocnemius-soleus muscles. It has been found that increasing doses of phentolamine given i.v. cause a decreasing pressor response until complete disappearance occurs at 2.5 mg/Kg. It is concluded that pressor response is present only when the adrenergic control system is effective and, therefore, it is due mainly to an increase in peripheral vascular resistances.

Animals↗
PubMed1987

Antagonism of cocaine-induced hepatotoxicity by the alpha adrenergic antagonists phentolamine and yohimbine.

The ability of the alpha adrenoreceptor antagonists phentolamine and yohimbine to antagonize cocaine-induced hepatotoxicity was determined in phenobarbital-induced B6C3/F1 mice. Hepatotoxicity was assessed by the histologic extent of necrosis, incidence of latent lethality and increases in serum alanine aminotransferase activity. The depression of hepatic glutathione levels also were measured. The administration of a single 5-mg/kg dose of phentolamine antagonized the decrease in glutathione levels and the elevation of aminotransferase activity caused by a 60-mg/kg dose of cocaine. Similar results were obtained in mice pretreated with the alpha-2 antagonist yohimbine. Whereas the duration of antagonism could be extended by administering a 30-mg/kg dose of yohimbine, the magnitude of the antagonism was not increased. In contrast to the experiments with the larger dose, multiple hourly doses of 2.5 mg/kg of yohimbine increased both the duration of antagonism and the magnitude of protection against the hepatotoxicity produced by cocaine. Yohimbine pretreatment reduced cocaine-induced latent lethality by 50%, but did not alter the time to lethality. The results of these experiments indicate that the alpha adrenoreceptor antagonist reduces the toxicity of cocaine rather than merely delaying its time of onset. This effect does not appear to result from an inhibition of the toxic metabolite(s) of cocaine, as a 10-fold molar excess of yohimbine failed to antagonize lipid peroxidation caused by in vitro incubation of cocaine with hepatic microsomes. Additional experiments in mice whose liver metabolism had not been induced by prior pretreatment with phenobarbital revealed that 60 mg/kg of cocaine lowered glutathione but was not hepatotoxic.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1978

Phentolamine infusion in cor pulmonale due to chronic obstructive pulmonary disease.

Continuous phentolamine infusion, produced a marked decrease in pulmonary arterial pressure and pulmonary vascular resistance with an increase in cardiac output, in the majority of a group of 13 patients with chronic obstructive pulmonary disease and cor pulmonale. Changes in vital capacity, forced expiratory volume in one second, arterial blood gas values and peripheral blood pressure were not significant except in one patient. The changes in the pulmonary circulation are probably due to the alpha blocking effect of phentolamine, although a direct effect of the drug on vascular smooth muscle can not be excluded.

Adult↗
PubMed1988

[Open multicenter study of the differential diagnosis of erectile dysfunction with a papaverine-phentolamine combination (BY023)].

We report the results of an open multicenter clinical trial with 115 patients. The results of a pharmacological test using intracavernously applied mixture of papaverine and phentolamine were compared with the results of a multidisciplinary evaluation of erectile dysfunction. Sensitivity and specificity of our test were determined. The injection of our drug solution caused an increase in tumescence and/or rigidity in all patients. The evaluation of the dose dependent erectile response makes it possible to distinguish between the three main pathogenetic principles: non-vascular, arterial and venous etiology of erectile dysfunction. The pharmacological test requires one to four intracavernous injections of 0.5-3.0 ml of the drug solution (7.5-45 mg papaverine hydrochloride, 0.25-1.5 mg phentolamine mesylate).

Adolescent↗
PubMed1985

[Hemodynamic effects of phentolamine in acute and chronic mitral insufficiency after myocardial infarction].

The haemodynamic effects of phentolamine, a selective alpha blocker, were studied in patients with severe mitral regurgitation and cardiac failure in the acute (Group I, 7 cases) or chronic (Group II, 7 cases) phase of myocardial infarction. After 1 hour's treatment a rise in cardiac index (+29 p. 100, p less than 0.001 and +36 p. 100, p less than 0.01), and systolic index (+19 p. 100, p less than 0.001 and +19 p. 100, p less than 0.05) were observed; the V wave of the pulmonary capillary pressure recording decreased (-32 p. 100, p less than 0.005; -26 p. 100, p less than 0.01). Oxygen transport also increased by an average of 36 p. 100, p less than 0.001, without a significant change in arterial pp O2. These results show that phentolamine improves the haemodynamics and decreases mitral regurgitation in the acute and in the chronic phases of myocardial infarction.

Acute Disease↗
PubMed1979

Effects of sodium nitroprusside, isosorbide dinitrate, isoproterenol, phentolamine and prazosin on hepatic venous responses to sympathetic nerve stimulation in the cat.

Hepatic blood volume was recorded by a plethysmographic technique in cats anesthetized with pentobarbital. The effects of three doses of each vasodilator drug were measured on arterial and portal pressures, hepatic blood volume in the denervated liver and on the portal pressure and hepatic venous responses to sympathetic nerve stimulation. Isosorbide dinitrate caused a small reduction in basal hepatic venous tone increasing hepatic blood volume by up to 15%; it had no effect on the responses to sympathetic nerve stimulation. Isoproterenol increased hepatic venous tone perhaps by stimulation of angiotensin formation and the responses to stimulation of the hepatic nerves were reduced because of this increased basal tone. Sodium nitroprusside produced a small decrease in basal venous tone and only large doses produced any reduction in the venous responses to hepatic nerve stimulation. The evidence that nitroprusside is a venodilator requires reexamination. Phentolamine had no effect on basal venous tone but markedly reduced the responses to sympathetic nerve stimulatiqn. When compared to phentolamine, prazosin produced comparable effects on arterial pressure but much less reduction in the hepatic venous responses to sympathetic stimulation. It is suggested that the alpha receptor blocking action of prazosin is selective for arterioles and this may explain the minor incidence of postural hypotension during clinical use.

Animals↗
PubMed1984

Hepatic microvascular regulatory mechanisms. V. Effects of lodoxamide tromethamine or phentolamine-HCl on vascular responses elicited by serotonin.

Initial changes in hepatic microvasculature and carotid (arterial) blood pressure were measured in anesthetized Sprague-Dawley rats receiving an endoportal injection or topical application of serotonin alone, or in combination with selected doses of lodoxamide tromethamine or phentolamine-HCl. Although infusion of 1.0 microgram per 100 g b.w. serotonin and/or 10 micrograms per 100 g b.w. lodoxamide produced no change in arterial blood pressure, 10 or 20 micrograms per 100 g b.w. serotonin evoked hypotension within 40 sec. During this period, in vivo microscopy of transilluminated livers revealed that 1.0 or 10 micrograms per 100 b.w. serotonin elicited constriction of portal venules and sinusoids, and a significant increase in the percentage of these microvessels containing decreased cellular flow. None of these responses was antagonized by 10 micrograms per 100 g b.w. lodoxamide. Topical application of 1.0, 10, or 20 micrograms serotonin provoked constriction of sinusoids and decreased sinusoidal and central venous perfusion, but no systemic hypotension. There was no significant difference in the magnitude of responses to these doses of serotonin alone or with 0.1 microgram lodoxamide; however, 100 micrograms phentolamine potentiated responses to 1.0 microgram serotonin. Given these results, and those of previous studies indicating that equivalent doses of these antagonists block mast cell degranulation or catecholamine-induced activation of alpha receptors, it is suggested that the vascular responses are mediated directly by serotonin and not indirectly by serotonin-evoked mast cell degranulation or alpha-adrenergic stimulation. The vascular receptor(s) triggered remain(s) to be elucidated.

Amino Acids↗
PubMed1983

[Effect of pretreatment with the alpha-adrenoblocker phentolamine and the beta-adrenoblocker inderal on the stress-induced decrease in adrenoreactivity of the portal vein].

The effect of the pretreatment with the alpha-adrenoblocker phentolamine and the beta-adrenoblocker inderal was studied on the disturbances of contractile function and adrenoreactivity which occurred after exposure to emotional-painful stress. The pretreatment of the animals exposed to emotional-painful stress with phentolamine prevented to a considerable degree the depression of portal vein contractility and raised adrenoreactivity of the smooth muscle that dramatically fell after emotional-painful stress to the basic level. Administration of inderal did not prevent the stress-induced disturbances. The data obtained suggest that the stress-induced injuring effect of catecholamine high concentrations is mediated via alpha-adrenoreceptors of portal vein smooth muscles.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Effects of nitrendipine (BAY e 5009), nifedipine, verapamil, phentolamine, papaverine, and minoxidil on contractions of isolated rabbit aortic smooth muscle.

The effects of nitrendipine, a new antihypertensive agent, have been examined using the isolated rabbit aortic strip stimulated with either noradrenaline (1.7 X 10(-8) - 1.7 X 10(-5) mol/L) or potassium (22.7-52.7 mmol/L). Nifedipine, verapamil, phentolamine, papaverine, and minoxidil were used as reference compounds. Nitrendipine and nifedipine had little effect on the contractions of the aortic strip induced by noradrenaline, but concentration-dependently inhibited contractions induced by potassium depolarisation (IC50) (3.1 X 10(-9) and 8.1 X 10(-9) mol/L, respectively). Verapamil had little effect on contractions induced by the highest concentration of noradrenaline (1.7 X 10(-5) mol/L) but inhibited contractions induced by lower concentrations of noradrenaline. Potassium-induced contractions were inhibited with an IC50 of 1.4 X 10(-7) mol/L. Phentolamine competitively inhibited noradrenaline-induced contractions, but had no effect on those induced by potassium. Papaverine inhibited both noradrenaline- and potassium-induced contractions with an IC50 of 2.5 X 10(-5) and 3 X 10(-5) mol/L, respectively. Minoxidil also inhibited both types of contractions, but only at very high concentrations (IC50 1.3 X 10(-3) and 1.8 X 10(-3) mol/L). I conclude that nitrendipine, like nifedipine, acts by inhibiting the depolarisation-induced influx of calcium ions into the vascular smooth muscle. There is no evidence for alpha-adrenoceptor-blocking activity, nor for papaverine-like vasodilator activity. Verapamil also appears to act by a calcium antagonistic action; but may, in addition, possess some alpha-adrenoceptor-blocking activity.

Animals↗